Williams Leanne M, Whitford Thomas J, Nagy Marie, Flynn Gary, Harris Anthony W F, Silverstein Steven M, Gordon Evian
Brain Dynamics Centre, Westmead Millennium Institute and Western Clinical School, University of Sydney, Westmead Hospital, Westmead NSW, Australia.
J Psychiatry Neurosci. 2009 Jul;34(4):303-13.
Schizophrenia may be understood as a disorder of neural synchrony. There is also increasing evidence that emotional and social cognitive impairments are central to this disorder. In patients with first-episode schizophrenia, we examined whether emotion perception is associated with disruptions to high-frequency (40 Hz) gamma synchrony and whether these disruptions predict self-regulatory adaptive compensations reflected in social cognitive behaviours.
We obtained electroencephalography recordings from 28 patients with first-episode schizophrenia and matched healthy controls during perception of facial emotion under both conscious and nonconscious conditions. We extracted gamma-band synchrony from the electroencephalogram. We also used behavioural measures of emotion identification, emotional intelligence, negativity bias and social function, along with ratings of first-episode schizophrenia symptoms. We analyzed group differences and predicted social cognition to assess the potential contribution of medication.
Within 200 ms poststimulus, patients with first-episode schizophrenia showed alterations in gamma synchrony during both conscious and nonconscious emotion perception. Stimulus-locked synchrony was reduced in patients, particularly over the temporal cortex, whereas complementary enhancements in absolute gamma synchrony (independent of stimuli) were more distributed over temporal and left parieto-occipital regions. This pattern of altered synchrony predicted poor performance on each measure of social cognition among these patients. Medication dosage did not correlate significantly with either gamma synchrony or behavioural measures in this group.
Limitations to our study include the lack of comparison between medicated and unmedicated patients or between types of medication.
These findings suggest that disruptions in integrative processing of motivationally important stimuli show promise as a potential biological marker of social cognitive impairments, present from the first episode of schizophrenia, and their outcomes.
精神分裂症可被理解为一种神经同步障碍。越来越多的证据表明，情绪和社会认知障碍是这种疾病的核心。在首发精神分裂症患者中，我们研究了情绪感知是否与高频（40赫兹）伽马同步性的破坏有关，以及这些破坏是否能预测社会认知行为中反映出的自我调节适应性补偿。
我们在有意识和无意识条件下对面部情绪进行感知时，获取了28名首发精神分裂症患者和匹配的健康对照者的脑电图记录。我们从脑电图中提取伽马波段同步性。我们还使用了情绪识别、情商、消极偏差和社会功能的行为测量方法，以及首发精神分裂症症状的评分。我们分析了组间差异并预测社会认知，以评估药物治疗的潜在作用。
在刺激后200毫秒内，首发精神分裂症患者在有意识和无意识情绪感知过程中均表现出伽马同步性的改变。患者的刺激锁定同步性降低，尤其是在颞叶皮质，而绝对伽马同步性（与刺激无关）的互补增强更多地分布在颞叶和左侧顶枕区域。这种同步性改变的模式预示着这些患者在各项社会认知测量中的表现较差。该组患者的药物剂量与伽马同步性或行为测量均无显著相关性。
我们研究的局限性包括未对服药患者和未服药患者或不同类型药物进行比较。
这些发现表明，对具有动机重要性的刺激进行整合处理的破坏有望成为社会认知障碍的潜在生物学标志物，这种障碍在精神分裂症首发时就已存在及其后果。
